75 research outputs found
Hyperréactivité bronchique provoquée par les b2-agonistes (mécanismes de signalisation intracellulaire)
No full textPARIS5-BU Saints-Pères (751062109) / SudocSudocFranceF
Validation of a predictive method for an accurate assessment of resting energy expenditure in medical mechanically ventilated patients
No full textObjective: Use comparison with indirect calorimetry to confirm the ability of our previously described equation to predict resting energy expenditure in mechanically ventilated patients.Design: Prospective, validation study. Setting: Eighteen-bed, medical intensive care unit at a teaching hospital. Patients: All adult patients intubated >24 hrs were assessed for eligibility. Exclusion criteria were clinical situations that could contribute to erroneous calorimetric measurements. Interventions: Resting energy expenditure was calculated using the original Harris-Benedict equations and those corrected for usual stress factors, the Swinamer equation, the Fusco equation, the Ireton-Jones equation, and our equation: resting energy expenditure (kcal/day) = 8 × weight (kg) + 14 × height (cm) + 32 × minute ventilation (L/min) + 94 × temperature (°C) − 4834. Measurements and Main Results: Resting energy expenditure was measured by indirect calorimetry for the 45 included patients. Resting energy expenditure calculated with our predictive model correlated with the measured resting energy expenditure (r2 = .62, p < .0001), and Bland-Altman analysis showed a mean bias of −192 ± 277 kcal/day, with limits of agreement ranging from −735 to 351 kcal/day. Resting energy expenditure calculated with the Harris-Benedict equations was more weakly correlated with measured resting energy expenditure (r2 = .41, p < .0001), with Bland-Altman analysis showing a mean bias of 279 ± 346 kcal/day between them and the limits of agreement ranging from −399 to 957 kcal/day. Applying usual stress-correction factors to the Harris-Benedict equations generated wide variability, and the correlation with measured resting energy expenditure was poorer (r2 = .18, p < .0001), with Bland-Altman analysis showing a mean bias of −357 ± 750 kcal/day and limits of agreement ranging from −1827 to 1113 kcal/day. The use of the Swinamer, Fusco, or Ireton-Jones predictive methods yielded weaker correlation between calculated and measured resting energy expenditure (r2 = .41, p < .0001; r2 = .38, p < .0001; r2 = .39, p < .0001, respectively) than our equation, and Bland-Altman analysis showed no improvement in agreement and variability between methods. Conclusions: The Faisy equation, based on static (height), less stable (weight), and dynamic biometric variables (temperature and minute ventilation), provided precise and unbiased resting energy expenditure estimations in mechanically ventilated patients
Population pharmacodynamic model of bicarbonate response to acetazolamide in mechanically ventilated COPD patients.
No full textInternational audienceABSTRACT: INTRODUCTION: Acetazolamide is commonly used in chronic obstructive pulmonary disease (COPD) patients with metabolic alkalosis. Little is known of the pharmacodynamics of acetazolamide in the critically ill. We undertook a pharmacodynamic modeling of bicarbonate response to acetazolamide in COPD patients under mechanical ventilation. METHODS: This observationnal, retrospective study included 68 invasively ventilated COPD patients who received one or multiple doses of 250 or 500 mg of acetazolamide during the weaning period. Among the 68 investigated patients, 207 time-serum bicarbonate observations were available for analysis. Population pharmacodynamics was modeled using a non linear mixed effect model. The main covariates of interest were baseline demographic data, simplified acute physiology score II (SAPS II) at intensive care unit (ICU) admission, cause of respiratory failure, co-prescription of drugs interfering with the acid-base equilibrium, and serum concentrations of protein, creatinin, potassium and chloride. The effect of acetazolamide on serum bicarbonate levels at different doses and in different clinical conditions was subsequently simulated in silico. RESULTS: The main covariates interacting with acetazolamide pharmacodynamics were SAPS II at ICU-admission (P = .01), serum chloride (P 500 mg twice daily is required to reduce serum bicarbonate concentration > 5 mmol/L in presence of high serum chloride levels or co- administration of systemic corticosteroids or furosemide. CONCLUSIONS: This study identified several covariates that influenced acetazolamide pharmacodynamics and could allow a better individualization of acetazolamide dosing when treating COPD patients with metabolic alkalosis
False Positive Ethylene Glycol Determination by Spectrophotometry in the Presence of Severe Lactic Acidosis and Ketosis
No full textEpinephrine Dose Has a Preventive Effect on the Occurrence of Stress Ulcer-Induced Gastrointestinal Bleeding in Critically Ill Patients
No full textEffect of severe acidosis on vasoactive effects of epinephrine and norepinephrine in human distal mammary artery
No full textObjectiveAcidosis is a very common pathologic process in perioperative management. However, how to correct severe acidosis to improve the efficacy of vasoconstrictors in hemodynamically unstable patients is still debated. The present study investigated whether severe extracellular acidosis influences the vasoactive properties of vasoconstrictors on human isolated arteries.MethodsSegments of intact distal internal mammary arteries were removed from 41 patients undergoing artery bypass grafting. The arterial rings were washed in Krebs-Henseleit solution and suspended in an organ bath. The rings were set at a pretension equivalent of 100 mm Hg, and the relaxation response to 10 μM acetylcholine was verified. Concentration–response curves for epinephrine, norepinephrine, methoxamine (α1A/D-adrenoceptor agonist), phenylephrine (equipotent agonist of α1A/B-adrenoceptors), and clonidine (α2-adrenoceptor agonist) were achieved under control conditions (pH 7.40) and under acidic conditions by substitution of the Krebs-Henseleit solution with a modified solution.ResultsDecreasing the pH from 7.40 to 7.20, 7.0, or 6.80 did not significantly alter the potency and efficacy of epinephrine and norepinephrine, although the standardized effect size was sometimes large. Severe acidosis (pH 6.80) did not significantly change the potency and efficacy of phenylephrine and clonidine, although it increased the efficacy and potency of methoxamine (P < .001 and P = .04 vs paired control conditions, respectively).ConclusionsExtracellular acidosis did not impair the vasoactive properties of epinephrine and norepinephrine in human medium-size arteries until pH 6.80. The results of the present study also suggest that acidosis might potentiate arterial responsiveness to vasoconstrictors, mostly by way of the α1D-adrenoceptor
Mechanical Stretch Modulates WNT2 Expression And Increases Airway Basal Tone Via RhoA-kinase Signaling Pathways In Human Isolated Bronchi
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